Changes in the mechanisms of brain adaption during postnatal ontogeny of rats exposed to prenatal hypoxia

Abstract

We have previously shown that acute hypoxia during embryogenesis impaired learning and memory processes during rat ontogeny [1]. These impairments could be related to changes in the structural and functional properties of neuronal networks of the cerebral cortex, specifically, with neurotransmission and structural intercellular interactions, because the number of neural elements in the hippocampus and the cerebral cortex in the adult rats that were exposed to hypoxia during embryogenesis were similar to the control values. It is known that impairments in cognitive functions and changes in amyloid precursor protein metabolism that are specific for the progress of dementia or Alzheimer’s disease are associated with a decrease in the expression of synaptophysine (a protein of presynaptic terminals) and the actin-associated spine protein synaptopodine [2]. A decrease in the expression of synaptopodine may result in disturbances of cytoskeleton formation in labile dendritic spines and a decrease in the plasticity of neuronal networks [3, 4]. The purpose of this study was comparative analysis of the synaptopodine distribution in the cortex and hippocampus during ontogeny in the control rats and the rats that had undergone prenatal hypoxia. On the basis of immunohistochemical data, we have demonstrated that prenatal exposure of rats to hypoxia leads to a decrease in the number of mobile synaptopodine-positive dendritic spines in the neuropile of cortical areas of the rat brain. These data demonstrate changes in the adaptive properties of neuronal networks and can explain disturbances in cognitive functions.